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Reduction in pulmonary fibrosis in vivo by halofuginone
Year:
1996
Authors :
Pines, Mark
;
.
Volume :
154
Co-Authors:
Nagler, A., Hadassah Univ. Hospital, Ein Kerem, P.O. Box 12000, Jerusalem 91120, Israel
Firman, N.
Feferman, R.
Cotev, S.
Pines, M.
Shoshan, S.
Facilitators :
From page:
1082
To page:
1086
(
Total pages:
5
)
Abstract:
Pulmonary fibrosis is a disorder causing a high mortality rate for which therapeutic options are limited. Therefore, the effect of halofuginone, a novel inhibitor of collagen type I synthesis, on bleomycin-induced pulmonary fibrosis was studied in rats. Pulmonary fibrosis was induced by intraperitoneal injections of bleomycin for seven consecutive days, and halofuginone was administered intraperitoneally every second day during the entire experimental period of 42 d. Collagen determination in the lungs and the examination of histologic sections showed that halofuginone significantly reduced fibrosis relative to the untreated control rats. We conclude that halofuginone is a potent in vivo inhibitor of bleomycin-induced pulmonary fibrosis, and that it may potentially be used as a novel therapeutic agent for the treatment of this dysfunction.
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DOI :
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
30708
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:56
Scientific Publication
Reduction in pulmonary fibrosis in vivo by halofuginone
154
Nagler, A., Hadassah Univ. Hospital, Ein Kerem, P.O. Box 12000, Jerusalem 91120, Israel
Firman, N.
Feferman, R.
Cotev, S.
Pines, M.
Shoshan, S.
Reduction in pulmonary fibrosis in vivo by halofuginone
Pulmonary fibrosis is a disorder causing a high mortality rate for which therapeutic options are limited. Therefore, the effect of halofuginone, a novel inhibitor of collagen type I synthesis, on bleomycin-induced pulmonary fibrosis was studied in rats. Pulmonary fibrosis was induced by intraperitoneal injections of bleomycin for seven consecutive days, and halofuginone was administered intraperitoneally every second day during the entire experimental period of 42 d. Collagen determination in the lungs and the examination of histologic sections showed that halofuginone significantly reduced fibrosis relative to the untreated control rats. We conclude that halofuginone is a potent in vivo inhibitor of bleomycin-induced pulmonary fibrosis, and that it may potentially be used as a novel therapeutic agent for the treatment of this dysfunction.
Scientific Publication
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